The potential role of unregulated autonomous bladder micromotions in urinary storage and voiding dysfunction; overactive bladder and detrusor underactivity.

The potential role of unregulated autonomous bladder micromotions in urinary storage and voiding dysfunction; overactive bladder and detrusor underactivity.
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DOI:
10.1111/bju.13598
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发表时间:
2017-01
期刊:
影响因子:
4.5
通讯作者:
Fry CH
Fry CH
中科院分区:
医学2区
文献类型:
--
作者:
Drake MJ;Kanai A;Bijos DA;Ikeda Y;Zabbarova I;Vahabi B;Fry CH

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离体膀胱表现出自主微运动,随膀胱膨胀而增加,产生感觉神经活动,并在尿功能障碍模型中发生改变。由自主活动引起的膀胱内压力通常反映三个关键变量;微动起始的程度、微动传播的距离和膀胱整体张力。在体内,这些变量从属于中枢神经系统的传出驱动。在排尿周期储存阶段,传出抑制使自主活动通常处于低水平,在维持顺应性的同时可能发出“饱腹状态”的信号。在排尿期,质量传出兴奋引起全身收缩(全身运动启动)。在下尿路功能障碍中,膀胱的传出控制可能受损,例如由于外周“斑片状”去神经支配。在这种情况下,传出抑制的丧失可能导致不受调节的微运动性和传入刺激,易导致尿急。如果去神经支配相对较轻,对排尿的有害影响可能较低,因为邻近的神经支配区可能能够与传出神经驱动同步启动微运动,因此即使去神经支配区也可以促进排尿收缩。去神经支配越严重,这将变得越来越低效,因此触发的微运动性传播能力足以使去神经支配区域参与排尿的能力下降,因此排尿收缩越来越呈现出活动不足的特征。总之,双传出神经支配(抑制性和兴奋性)的外周覆盖减少,损害了微运动性开始和传播的调节,可能导致膀胱过度活动,随着进展,逼尿肌活动不足。
The isolated bladder shows autonomous micromotions, which increase with bladder distension, generate sensory nerve activity, and are altered in models of urinary dysfunction. Intravesical pressure resulting from autonomous activity putatively reflects three key variables; the extent of micromotion initiation, distances over which micromotions propagate, and overall bladder tone. In vivo, these variables are subordinate to the efferent drive of the central nervous system. In the micturition cycle storage phase, efferent inhibition keeps autonomous activity generally at a low level, where it may signal “state of fullness” while maintaining compliance. In the voiding phase, mass efferent excitation elicits generalized contraction (global motility initiation). In lower urinary tract dysfunction, efferent control of the bladder can be impaired, for example due to peripheral “patchy” denervation. In this case, loss of efferent inhibition may enable unregulated micromotility, and afferent stimulation, predisposing to urinary urgency. If denervation is relatively slight, the detrimental impact on voiding may be low, as the adjacent innervated areas may be able to initiate micromotility synchronous with the efferent nerve drive, so that even denervated areas can contribute to the voiding contraction. This would become increasingly inefficient the more severe the denervation, such that ability of triggered micromotility to propagate sufficiently to engage the denervated areas in voiding declines, so the voiding contraction increasingly develops the characteristics of underactivity. In summary, reduced peripheral coverage by the dual efferent innervation (inhibitory and excitatory) impairs regulation of micromotility initiation and propagation, potentially allowing emergence of overactive bladder and, with progression, detrusor underactivity.
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